Okan Onur Turgut

Comparative effects of levosimendan and dobutamine on right ventricular function in patients with biventricular heart failure

Severe heart failure represents a major source of morbidity and mortality. Poor right ventricular function is an independent prognostic marker for mortality in patients with chronic heart failure. In this study, levosimendan (L) and dobutamine (D) in patients with severe chronic biventricular failure were compared. Forty consecutive patients, who were judged for inotropic therapy by their primary physicians, with acutely decompensated systolic heart failure and having moderate-to-severe right ventricular dysfunction with right ventricular fractional area change of ≤24%m were randomized to L and D in a 2:1 fashion. Echocardiographic parameters including tricuspid annular motion and clinical issues were considered. Mean age and sex distribution were not different between the two groups. After the infusion, ejection fraction improved and systolic pulmonary artery pressure decreased significantly in both arms. Longitudinal systolic function of tricuspid annulus improved significantly better in patients with L compared to patients with D (15% ± 12% vs. 2% ± 6% improvement, P < 0.001). Furthermore, L improved both 24-h urine output and creatinine, whereas D showed only a small, but significant improvement in urine output without any improvement in the creatinine levels. Levosimendan seems to offer more beneficial effects compared to dobutamine in a specific group of patients with biventricular failure.

Sleep quality among relatively younger patients with initial diagnosis of hypertension: dippers versus non-dippers.

Background. Sleep is a basic physiological process. Normal sleep yields decrease in sympathetic activity, blood pressure (BP) and heart rate. Those, who do not have expected decrease in their BP are considered “non‐dippers”. We aimed to determine if there was any association between the non‐dipping status and sleep quality, designed a cross‐sectional study, and enrolled and evaluated the sleep quality of relatively young patients with an initial diagnosis of hypertension. Methods. Seventy‐five consecutive patients, diagnosed to have stage 1 hypertension by their primary physicians, were referred to our study. Patients had newly diagnosed with stage 1 hypertension. Patients with a prior use of any anti‐hypertensive medication were not included. Eligible patients underwent the Pittsburgh Sleep Quality Index (PSQI), which has an established role in evaluating sleep disturbances. All patients underwent ambulatory BP monitoring. Results. There were 42 non‐dipper patients (mean age = 47.5±11.9 years, 24 male/18 female), as a definition, 31 dipper hypertensive patients (mean age = 48.5±12.8 years, 21 male/10 female) and two with white coat hypertension. Daytime systolic and diastolic mean BPs were not significantly different between the two groups. Night‐time mean systolic and diastolic BPs were significantly higher in non‐dippers compared with dippers. PSQI scores, globally, were significantly higher in non‐dippers compared with dippers. Total PSQI score was not correlated with body mass index. It was noticed that, individually, sleep quality, sleep efficiency and sleep disturbance scores were significantly higher in non‐dippers. Being a poor sleeper in terms of high PSQI score (total score>5) was associated with 2.955‐fold increased risk of being a non‐dipper (95% confidence interval 1.127–7.747). Conclusion. We showed that the risk of having non‐dipping hypertension, a risk factor for poor cardiovascular outcomes among hypertensive individuals, was tripled (odds ratios) among poor sleepers. We think that evaluating sleeping status and sleep quality among the hypertensive population may help unmask non‐dipper hypertension, enabling physicians to treat appropriately.

Impact of beta-blockers on sleep in patients with mild hypertension: a randomized trial between nebivolol and metoprolol.

IntroductionSleep is an innate and essential part of human life. Various aspects of sleep are negatively affected by beta-blockers. We compared the impact of two beta-blockers, metoprolol succinate (extended release) and nebivolol, on sleep quality in patients with stage 1 hypertension.MethodsThis was a prospective, randomized, open-label, parallel-group study. Eligible patients were administered the Pittsburgh Sleep Quality Index (PSQI) questionnaire by a blinded interviewer and were randomized to receive metoprolol (starting dose 25 mg) or nebivolol (starting dose 2.5 mg) once daily for 6 weeks. The first dose was administered before patients left the clinic. Visits were scheduled for 1, 2, 4, and 6 weeks after the initiation of therapy. At the end of the study, patients were readministered the PSQI questionnaire by the same interviewer, as before blinded to treatment allocation.ResultsA total of 22 patients in the nebivolol group and 17 patients in the metoprolol group completed the study and were included in the data analysis (mean age of patients, 40.7 years). At study entry, systolic blood pressure (BP), diastolic BP, and PSQI scores were similar in the two groups. Over 6 weeks of treatment, systolic and diastolic BP normalized in both groups. Global PSQI score improved significantly in patients in the nebivolol group, whereas it worsened in the metoprolol group. The difference in effect of two beta-blockers was statistically significant (P<0.001).ConclusionNebivolol was associated with improved sleep (as assessed by the PSQI), whereas metoprolol was associated with a worsening of sleep characteristics.

Avicenna: Messages from a great pioneer of ancient medicine for modern cardiology

Avicenna deserves to be remembered for his contributions to the field of cardiovascular medicine. His masterpiece, the Canon of Medicine, has served as an essential medical encyclopedia for scholars in the Islamic territories and Europe for almost a millennium. The Canon, which is a general treatise on medicine, consists of five books. The eleventh section of the third book principally deals with various kinds of heart diseases, their causes, effects, and treatment. He has expressed that the heart is the noblest and the best of all the chief organs of the human body. Avicenna has tried to find out the causes of heart diseases and classify them in accordance with the different signs and symptoms. His legacy will continue to inspire his modern colleagues in investigating heart diseases.

Evaluation of Tumor Markers CA-125 and CEA in Acute Myocardial Infarction

Serum carbohydrate antigen (CA-125) and carcinoembryonic antigen (CEA) have always been of clinical importance in the diagnosis and follow-up of various tumors. This study was devised to investigate the relationship between these tumor markers and acute myocardial infarction (MI). Seventy consecutive cases (59 male patients with a diagnosis of acute ST segment elevation MI and 11 male patients with a diagnosis of non-ST segment elevation MI; mean age, 57±8.2 y) were admitted to the University Medical Center and were included in this study as “the patient group.” All patients in the patient group underwent transthoracic echocardiographic examination on the third day of hospitalization. On the basis of echocardiographic findings, these 70 patients were grouped according to left ventricular ejection fraction (EF) values; EF < 55% (group 1) (n=40) and EF≥55% (group 2) (n=30). Other parameters, including systolic pulmonary artery pressure (sPAP) and mean pulmonary artery pressure (mPAP), were also measured on transthoracic echocardiography. Serial blood samples (for follow-up of myocardial enzymes (eg, creatine kinase MB [CKMB], troponin I [TnI], troponin T, and other routine parameters) were drawn from each patient. Serum concentrations of CEA and CA-125 measured at the 72nd hour of hospitalization and peak serum concentrations of CKMB and TnI in the patient group were collected for comparison between subgroups (groups 1 and 2) and with “the control group”, which included 30 subjects (mean age, 54±7.6 y) with no history or evidence of overt cardiac disease and with normal echocardiographic findings. The presence of any condition characterized by potential elevations in CA-125, CEA, and myocardial enzymes (CKMB, TnI) was considered an exclusion criterion. Patients included in patient groups 1 and 2 differed significantly in terms of mean EF, mean sPAP, mean mPAP, and mean CA-125 values (P < .001 for CA-125;P < .05 for the other values). EF was found to be negatively correlated with sPAP (r=-0.692,P=.000) and mPAP (r=-0.393,P=.001). EF was also negatively correlated with CA-125 (r=-0.557,P=.000). A positive correlation was noted between CA-125 and sPAP (r=0.396,P=.001) and between CA-125 and mPAP (r=0.754,P=.000). A statistically significant difference was identified between the patient and control groups with regard to values for EF, PAP, CA-125, and myocardial enzymes (CKMB and TnI) (P < .05 for mPAP;P < .001 for the other values). The serum concentration of CA-125, but not of CEA, may be elevated in those with acute MI compared with normal subjects. Regardless of the presence of pulmonary hypertension, elevations in CA-125 during myocardial infarction were significantly correlated with the severity of left ventricular systolic dysfunction on transthoracic echocardiography.

CA125 levels among patients with advanced heart failure: an emerging independent predictor for survival.

Serum CA125, a high-molecular weight glycoprotein, is a tumor marker widely used for the diagnosis and follow-up of patients with ovarian cancer in clinical practice. Recently, increased serum CA125 values, in parallel with catecholamines and natriuretic peptides, have also been documented in patients with heart failure. As far as the relationship between CA125 and cardiac dysfunction is concerned; interleukin-6, interleukin-10, and tumor necrosis factor-α, which are all elevated in heart failure, might play a pivotal role, since there are data suggesting that the proliferation of CA125-producing cells is induced by proinflammatory cytokine network. However, little is known about the biologic role of this substance: whether it simply reflects the increased activation of the cytokine pathway (or other pathophysiologic pathways), or whether CA125 is an active substance truly responsible for myocardial and/or peripheral dysfunction. Further insight to the precise determinants for increased CA125 levels in this population would help establish the clinical usefulness of this emerging marker in predicting survival.

Association of P wave duration and dispersion with the risk for atrial fibrillation: Practical considerations in the setting of coronary artery disease

P wave dispersion (PWD) is defined as the difference between maximum P wave duration (Pmax) and minimum P wave duration recorded from multiple surface electrocardiogram (ECG) leads. An increase in PWD indicates heterogeneous intraatrial and interatrial conduction and discontinuous anisotropic propagation of sinus impulses, providing a substrate that favors reentry mechanisms. Prolonged Pmax and increased PWD have been suggested to represent independent predictors for atrial fibrillation (AF). The distinctive atrial electrophysiological peculiarity featured by slow interrupted propagation of atrial impulses could be reflected by an increase in PWD predisposing to AF. Coronary artery disease (CAD) is also a well-known risk factor for AF. There are some potential mediators between CAD and AF. The noninvasive nature of P wave duration and PWD with their comparative simplicity makes these parameters attractive options; however, standards involving precise assessment are still lacking. Further exploration of the exact determinants for P wave duration and PWD would help establish the practical usefulness of these surface ECG markers in estimating the risk for AF occurrence and recurrence.

Clinical importance of elevated CK-MB and troponin I levels in congestive heart failure

Myocyte necrosis has been considered to play a fundamental role in the pathophysiology of congestive heart failure (CHF), which has usually evolved as a consequence of depletion of compensatory mechanisms and contractile reserve of myocardium. Elevated levels of creatine kinase MB (CK-MB) and troponin I (Tn-I) have been regarded as biochemical markers of myocyte necrosis. This study was planned to investigate the specificity and sensitivity of Tn-I and CK-MB in CHF and to examine the correlation of these markers with disease severity. A total of 104 patients (38 female, 66 male; mean age, 66 y [range, 36–89]) with symptoms and signs of heart failure on admission and with a reduced left ventricular ejection fraction (EF; by transthoracic echocardiography) were labeled “the patient group”, and 58 patients (40 female,18 male; mean age, 61 y [range, 34–77]) with no signs or symptoms of CHF and with a normal EF detected by transthoracic echocardiography were included in the study as “the control group.” Left ventricular EFs, end-diastolic diameters, and end-systolic diameters of patients in both groups were measured. Blood samples were drawn from all patients in both groups on admission, so that levels of CK-MB and Tn-I could be measured. All patients in both groups also underwent coronary angiography. Conditions leading to elevation of CK-MB or Tn-I were considered exclusion criteria. The 2 groups failed to show any significant differences in terms of mean age and the presence of coronary artery disease, hypertension, or diabetes mellitus (P > .05). Mean EF in the patient group was lower than that in the control group (P < .05). Mean CK-MB and Tn-I in the patient group were significantly higher than in the control group (P < .05). In the patient group, hypertensive patients were found to have significantly higher mean values of CK-MB than were seen in normotensive patients in the same group (P < .05). In the patient group, 52 cases were considered to be class I-II (New York Heart Association [NYHA]) (group 1), and 52 were considered to be class III-IV (group 2). Group 1, group 2, and the control group did not differ significantly from one another with regard to the presence of coronary artery disease, hypertension, and diabetes mellitus (P > .05).The mean EF in group 2 was significantly lower than that in group 1 and in the control group (P < .05); the mean EF in group 1 was significantly lower than that in the control group (P < .05). Group 1 values did not differ significantly from those of group 2 or the control group in terms of enzymatic markers (P > .05), but group 2 had significantly higher mean values of CK-MB and Tn-I than were noted in the control group (P < .05). The uphill course of CK-MB and Tn-I values from the control group to group 2 (NYHA class III-IV) was statistically significant (P< .05). Serum concentrations of CK-MB and Tn-I may become elevated in severely symptomatic patients with CHF (particularly NYHA class III-IV), demonstrating a relationship between clinical severity of the disease and elevation of myocardial enzymes (CK-MB and Tn-I).

Genetic basis of sudden cardiac death due to emotional trauma in apparently healthy individuals

Abstract Several mechanisms underlying sudden deaths due to emotional trauma have been propounded. Emotional trauma has been known to be associated with hyperactivation of some physiyological systems including sympathetic system that may directly trigger malign arrhythmic events in arrhythmia-prone subjects or lead to some clinically serious conditions including acute coronary syndromes, Tako-tsubo cardiomyopathy (TTC) etc. that may have the potential to trigger sudden cardiac death (SCD). Besides these well known effects, emotional trauma may be associated with SCDs due to some genetically determined arrhythmogenic conditions including ion channelopathies (overt or obscure), particularly in relatively young victims with no apparent etiology of SCD suggesting thorough evaluation and genetic screening of family members of these victims for prevention of SCD.

Association of γ-Glutamyltransferase with Cardiovascular Risk: A Prognostic Outlook

gamma-Glutamyltransferase (GGT), an enzyme responsible for the extracellular catabolism of antioxidant glutathione, may explicitly participate in atherogenesis. Several population-based studies have documented strong cross-sectional associations between serum GGT concentrations and certain cardiovascular risk factors, irrespective of alcohol consumption. The mechanism underlying these associations remains largely enigmatic. Considerable association of high-sensitivity C-reactive protein, a major inflammatory marker for cardiovascular risk, with GGT and other cardiovascular risk factors has been described, implying that elevation of serum GGT (conceivably acting as a marker of oxidative stress) is correlated with subclinical microinflammatory response involved in the pathogenesis of atherosclerosis. It is also relevant to assess whether the prognostic impact of a novel risk marker can be influenced by therapeutic intervention, thus decreasing the occurrence of cardiovascular events. Subtle gradations in serum GGT may help predict long-term cardiovascular prognosis, and the supplementary GGT determination to conventional testing has potential implications for screening those at increased cardiovascular risk who may benefit from prophylactic measures and require enhanced therapeutic effort. It has been reported that serum GGT may contribute to the accumulation of GGT activity inside the plaque. Further comprehension is, however, needed about the relationship of GGT activity inside the plaque with inflammatory biomarkers, plasma lipoproteins, and other independent determinants to define the most risky combination and improve the prognostic stratification of patients.